Stretch marks, medically known as striae, do not darken when exposed to sunlight like the surrounding skin. Striae are a widespread form of skin alteration resulting from rapid stretching of the skin, such as during pregnancy, growth spurts, or rapid weight changes. This lack of color change creates a noticeable visual contrast when the surrounding skin tans. The explanation lies in the fundamental biological difference between healthy skin and scar tissue.
How Healthy Skin Produces a Tan
Tanning is the body’s natural defense mechanism against the harmful effects of ultraviolet (UV) radiation from the sun. When UV rays penetrate the epidermis, specialized cells called melanocytes are stimulated to produce pigment. This stimulation increases the synthesis of melanin.
Melanin is packaged into melanosomes, which are then distributed to the surrounding skin cells, or keratinocytes. The pigment darkens the skin, acting as a natural broad-spectrum filter that absorbs UV energy. This prevents UV rays from reaching the deeper layers and damaging cellular DNA. This protective process is what we recognize visually as a tan.
The Structural Composition of Stretch Marks
Stretch marks are a form of dermal scarring that occurs when the skin is rapidly stretched beyond its physical limits. This abrupt tension causes the support structures in the dermis, the middle layer of the skin, to rupture. The essential fibers, collagen for strength and elastin for elasticity, become damaged and disorganized.
Initially, these marks are often red, pink, or purplish (striae rubrae) due to inflammation and the presence of blood vessels. Over time, the inflammation subsides, the blood vessels narrow, and the area heals into striae albae. These mature marks are white or silvery, atrophic, and resemble scar tissue. Histologically, the white marks show epidermal thinning and dense, parallel bundles of collagen that are structurally different from the surrounding skin.
Why Scar Tissue Lacks Tanning Ability
The primary reason stretch marks do not tan is that the scar tissue lacks the necessary pigment-producing machinery. The trauma that created the stretch mark damages the dermal-epidermal junction, the boundary layer where the melanocytes reside. As the skin heals and forms scar tissue, the fibrous repair process fails to restore the population of melanocytes.
In the absence of these melanocytes, the area cannot produce melanin regardless of UV exposure. Furthermore, the white stretch mark exhibits epidermal atrophy, meaning the outer skin layer is thinned. The underlying structure is replaced with disorganized collagen bundles. This structural alteration confirms that the stretch mark is a permanent scar biologically incapable of initiating the tanning response.
Options for Reducing Visual Contrast
Since the stretch mark itself cannot tan, the visual contrast is heightened when the surrounding healthy skin darkens. One effective strategy for minimizing this difference is to strictly limit the tanning of the adjacent normal skin. This is accomplished by consistently applying a high-SPF, broad-spectrum sunscreen to all exposed areas, or by covering the region entirely.
Another practical approach is cosmetic camouflage, which involves using topical products to match the colors. Self-tanners contain the active ingredient dihydroxyacetone (DHA), which creates a temporary color change by reacting with proteins on the skin’s surface. This process does not rely on functional melanocytes. These products can be applied to the stretch mark to help it blend with the naturally tanned skin. Dermatological procedures, such as laser therapy or microneedling, aim to improve the texture by stimulating collagen and elastin production, but they do not guarantee the restoration of tanning ability.